Non-rheumatic atrial fibrillation (NRAF) is associated with thromboembolic complications such as strokes. For example, when a thrombus or embolus occludes a vessel supplying blood to the brain, a stroke may result causing temporary or lasting paralysis of a part of the body or, in severe cases, death. Blockage of other blood vessels can occur as well causing attendant health concerns, including heart attack or gangrene. Presently, a five percent risk of stroke per year in a largely aging population causes NRAF to be a significant health concern. Given the potentially irreversible and destructive nature of such blood vessel occlusion, safe and effective methods are needed to eliminate embolic material like blood clots from the vascular system, some of which may be formed within an atrial appendage of the heart.
The left atrial appendage forms a small protrusion which is attached to the lateral wall of the left atrium between the mitral valve and the root of the left pulmonary vein and normally contracts along with the left atrium. Atrial fibrillation is a cardiac condition wherein the atria beat faster than the ventricles, causing the ventricles to contract irregularly and consequently eject less blood into the vascular system. A major problem associated with atrial fibrillation is pooling of blood in the left atrial appendage.
During NRAF the left atrial appendage may not fully contract, leaving stagnant blood within the left atrial appendage. In turn, the stagnant blood may create a condition favorable to the formation of blood clots within the left atrial appendage. Such clots may travel from the left atrial appendage into the left atrium and into the vascular system, thereby increasing the danger of stroke or cardiac blockage.
Traditional treatments to mitigate the risks posed by blood clots include the use of anticoagulants to dissolve the clots. For example, recently published results from stroke prevention trials suggest that prophylaxis with anticoagulation is beneficial to patients with non-rheumatic, non-valvular atrial fibrillation. Current therapeutic interventions include anticoagulation with coumedin. In addition, therapeutic interventions include the use of atrial rate regulating medications. However, both of these treatment approaches pose potential complications such as internal bleeding, as well as other negative side effects caused by the rate regulating therapeutic agents.
In addition to pharmacological treatments, complex radical surgical methods are available to treat atrial fibrillation. Such treatments include, for example, atrial incisions or removal of the left atrial appendage, which have been attempted in a limited, experimental way. Such approaches are highly invasive and pose a risk of mortality to the patient. Thus, a pressing need exists for means by which the formation of blood clots the left atrial appendage is substantially deterred while preventing the migration of any blood clots which may form from entering the vascular system.
U.S. Pat. No. 6,152,144 to Lesh et al., for example, discloses a device and method for obliterating or occluding a body cavity or passageway. Specifically, the patent to Lesh is directed to a device and method for obliterating or occluding the left atrial appendage of a patient's heart. In one embodiment, Lesh et al. disclose a frame structure having a barrier or mesh material disposed over it to act as a barrier to the passage of embolic material.
However, Lesh et al. do not disclose a device or method suited to treat atrial fibrillation, or other arrhythmias of the heart, to thereby prevent the formation of clots in the left atrial appendage. As such, the barrier embodiment of Lesh et al. permits ongoing formation of clots within the left atrial appendage, which may eventually occlude the barrier material to prevent fluid flow as well as embolic material flow through the occluded barrier. Such a situation may present a health concern as the left atrial appendage contracts and the blood enclosed therein is unable to exit the left atrial appendage. Such contraction may result in an increased pressure in the left atrial appendage capable of weakening the wall of the left atrial appendage. Additionally, as the barrier embodiment of Lesh et al. does not prevent the formation of clots, it is possible that the volume of the left atrial appendage may eventually be filled with coagulated blood. Thus, filtering alone poses possible added health concerns.
Regarding the treatment of atrial fibrillation, it is known to use a pacemaker, for example, as disclosed in U.S. Pat. No. 6,178,351 B1 to Mower. Mower discloses a pacemaker that is capable of pacing the atria from multiple sites, but does not address prevention of migration of embolic material within the vascular system. Moreover, neither Mower nor Lesh suggests combining a pacer with an embolic barrier for use in the heart.
Accordingly, there is a need for an apparatus for mitigating the risks associated with emboli originating in the left atrial appendage and also for reducing the tendency of such emboli, such as blood clots, to form therein.